77% of Late Onset Alzheimer’s Disease have NO genetic connection

If a genetic mutation predisposes you to Alzheimer’s, then we would see a much stronger familial link for this disease – which we don’t.  

What we do see is pretty shocking.  Of the multiple large scale studies we reviewed, 77% of Late Onset AD cases (referred to as LOAD) have absolutely NO family history of AD!  Which makes the slight (16%) of AD cases whose mother also died of the disease a bit underwhelming

HERE IS THE DATA THAT WILL LEAVE YOU SLEEPING BETTER AT NIGHT¹:

A review of 3,342 confirmed AD cases shows:  

*No Family History represented 77% of the cases 

*Having a mother with AD represented 16% of the cases 

*Having a father with AD represented 6% of the cases  

Yet many researchers suspect that Alzheimer’s Disease is genetic.

When we look at Alzheimer’s Disease from genes as being the driver, this disease can be classified in one of two ways:

• PROVEN TO BE GENETICALLY DRIVEN: Early Onset (EOAD) – which strikes before the age of 65 and is estimated to affect 1% of all Alzheimer’s diagnosis. It has been determined to be caused by the presence of 3 rare genes: 

Amyloid Precursor Protein (APP) which is located on chromosome 21

Presenilin 1 (PSEN1) which is located on chromosome 14

Presenilin 2 (PSEN2) which is located on chromosome 1

• SUGGESTED TO BE GENETICALLY DRIVEN: Late Onset (LOAD) – which strikes after the age of 65 – is estimated to affect 99% of all Alzheimer’s diagnosis. It is most associated with the risk gene called APOE-4 for reasons not fully understood by science to date.

The significantly more common form of Alzheimer’s – LOAD – is not so clear in its origin.  Over time it has come clear that three main lines of reasoning are emerging – which in turn become hypothesis until they are proven or disproven.  

The three main Alzheimer’s Disease Hypotheses being studied around the world are: 

1. APOE-4 Gene Variant Theory: aka the “mutating gene hypothesis”
2. Amyloid Beta Cascade Theory: aka the “protein-gone-rouge hypothesis” 
3. Opportunistic  Pathogen Theory: aka the “microbial hypothesis”  – which is being studied at The Alzheimer’s Legacy lab that our foundation is sponsoring at the University of Minnesota.

The first two theories hinge on the idea that the human body is the problem, that in the last 100 years changes to our DNA are now manifesting in diseases such as Alzheimer’s.

The last theory hinges on the idea that environmental factors (such as what we are eating, and our lifestyle choices) are the problem, that in the last 100 years changes to society are now manifesting in diseases such as Alzheimer’s.

1. Maternal transmission of Alzheimer’s disease: Prodromal metabolic phenotype and the search for genes  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033750/ ↩︎